Methods of estimating hormone-receptor interactions based on the ability of the hormone to induce a biological response have indicated that stimulation of steroidogenesis in normal and neoplastic Leydig cells occurs only when an apparent threshold level of hormone-receptor complex has formed. The size of the threshold is modified by theophylline (a drug known to inhibit phosphodiesterase) suggesting that it may be under the control of cyclic necleotides. Experiments are planned to investigate the possiblity that the threshold can be modified by other agents known to modify cyclic AMP metabolism at the levels of phosphodiesterase or adenyl cyclase. Attempts will also be made to alter the threshold by altering the total number of receptors per cell to determine if the threshold is due to a requirement that a given number of receptor sites be occupied or that a given fraction of receptor sites be occupied. Finally, efforts will be directed at learning what influence the level of intracellular cholesterol has on the size of the threshold since side chain cleavage of cholesterol is known to be a rate limiting step in steroidogenesis.